European Heart Journal Advance Access originally published online on November 30, 2004
European Heart Journal 2005 26(1):99-100; doi:10.1093/eurheartj/ehi030
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Letter to the Editor
What is ‘reperfusion injury’?: reply
online publish-ahead-of-print 30 November 2004 We agree with Dr Ostadal that the current terminology used to describe the range of changes induced by the reperfusion of myocardium which has undergone prolonged ischaemia can be both confusing and inadequate. While the spectrum of changes could be described under the umbrella term of ischaemia/reperfusion injury, this term itself is too broad as the pathophysiology of the resultant ischaemia/reperfusion substrate will depend on the severity, transmural extent, and duration of the pre-existing ischaemia, as well as on the type of reperfusion therapy used, the characteristics of the reconstituted flow (driving pressure), and the degree of microvascular injury.However, we would disagree with Dr Ostadal that experimental animal data do not mirror the findings in clinical practice. It is perhaps more the case that the appropriate experimental studies relevant to the substrates encountered in clinical practice are only currently being carried out or are yet to be performed. While much research in this field is examining changes at the molecular and cell membrane level, remarkably few studies are being performed in closed-chest experimental models, or in clinical practice, to examine the potential differences between thrombolytic and primary angioplasty revascularization. Such studies require the appropriate use of quantitative imaging techniques.
Turschner et al.1 in their closed-chest experimental animal study confirmed that full-pressure reperfusion of an acute transmural infarct causes immediate massive extracellular oedema which disrupts myocardial integrity. In an extension of this work, Streb et al.,2 attempting to simulate the result of clinical thrombo-lysis, have shown that the degree of extracellular oedema is diminished if there is a residual stenosis in the supplying artery and thus a reduced driving pressure in the reperfused epicardial vessel. Subsequent correlative clinical studies, in patients undergoing primary angioplasty for ST-elevation myocardial infarction, by Herbots et al.3 have shown that the degree of induced increase in wall thickness in the infarct zone is related to the transmurality of the infarct, as reflected in scar distribution detected by CMR late-enhancement imaging at 3–6 months post-infarction. Merli et al.,4 in an ongoing prospective clinical study, have compared the development of intramural oedema (reflected by the immediate increase in wall thickness) following primary coronary angioplasty versus changes induced by thrombolytic therapy in ST-elevation infarcts. They have shown that changes in wall thickness differ between the two reperfusion strategies, with little or no immediate increase in wall thickness in patients undergoing thrombolysis in whom there is a residual stenosis in the epicardial vessel, compared with the marked increase in wall thickness associated with successful primary angioplasty. Both Herbots and Merli have confirmed that, in the setting of a primary angioplasty procedure, a failure to record an immediate increase in wall thickness was highly suggestive of sub-optimal reperfusion in the long term. It is interesting to note that these clinical findings were predicted from the results of a series of prior experimental animal studies which set out to simulate the clinical substrate.
St George's Hospital
Department of Cardiology
Blackshaw Road
London
SW17 0QT
UK
E-mail address: george.sutherland{at}stgeorges.nhs.uk
Catholic University of Leuven
Department of Cardiology
University Hospital Gasthuisberg
Herestraat 49
3000 Leuven
Belgium
E-mail address: jan.dhooge{at}uz.kuleuven.ac.be
References
- Turschner O, D'hooge J, Dommke C et al. The sequential changes in myocardial thickness and thickening which occur during acute transmural infarction, infarct reperfusion and the resultant expression of reperfusion injury. Eur Heart J 2004;25;794–803.
[Abstract/Free Full Text] - Streb W, Marciniak M, Claus P et al. The wall thickness as a marker of artery status after the reperfusion therapy for acute myocardial infarction. An experimental study. (Abstract). Eur J Echocardiogr 2004; in press.
- Herbots L, Eroglu E, D'hooge J et al. Echocardiographic assessment of end-diastolic wall thickness can be used as a marker of reperfusion in transmural and partial thickness infarcts. (Abstract). Circulation 2004; 110(Suppl. III):713.
- Merli E, Sutcliffe S, Karu T et al. Changes in regional wall thickness and deformation indices in the acute infarct zone following either primary angioplasty or thrombolysis in patients with a ST elevation myocardial infarction. Do the resultant reperfused substrates differ? Eur J Echocardiogr 2004; in press.
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